Abstract
BackgroundUnderstanding the molecular mechanism of long non-coding RNAs (lncRNAs) in carcinogenesis is conducive for providing potential target for cancers. The role of FLVCR1-AS1 in breast cancer (BC) has not been probed yet.Materials and methodsqRT-PCR and western blot assays were used to estimate relevant expressions of mRNAs and proteins. CCK8, MTT and EdU were implemented to assess cell proliferation ability. TUNEL was performed to investigate cell apoptosis, whereas transwell assay was performed to test cell migration and invasion capacities. TOP/FOP Flash assay was conducted to determine the activity of Wnt/β-catenin pathway. Luciferase reporter, RNA pull down and RIP assays were performed to verify interaction between genes.ResultsFLVCR1-AS1 was abnormally up-regulated in BC cells. Silencing FLVCR1-AS1 inhibited cell proliferation, migration, invasion, yet accelerating apoptosis. Inhibition of miR-381-3p reversed the tumor restraining impacts of FLVCR1-AS1 depletion on BC progression. Additionally, CTNNB1 was recognized to be targeted by miR-381-3p. FLVCR1-AS1 aggravated BC malignant progression via up-regulation CTNNB1 through sponging miR-381-3p.ConclusionFLVCR1-AS1 regulates BC malignant behavior via sequestering miR-381-3p and then freeing CTNNB1, implying a promising target for BC therapy.
Highlights
Understanding the molecular mechanism of long non-coding RNAs in carcinogenesis is conducive for providing potential target for cancers
Li et al [15] discovered that long non-coding RNAs (lncRNAs) HOXC13-AS, which was significantly up-regulated in breast cancer (BC), enhanced cell proliferation ability through up-regulating PTEN expression via suppressing miR-497-5p
FLVCR1‐AS1 is aberrantly overexpressed in BC cells and silencing FLVCR1‐AS1 can dampen the malignant behavior of BC Firstly, qRT-PCR was carried out to explore the expression status of FLVCR1-AS1 in BC cells
Summary
Understanding the molecular mechanism of long non-coding RNAs (lncRNAs) in carcinogenesis is conducive for providing potential target for cancers. Breast cancer (BC), as one of the most frequently diagnosed cancer types in women, accounts for approximately 29% of all female malignancy cases [1, 2] Clinical advances, such as mastectomy, radiotherapy, chemotherapy and even systemic treatment have been achieved in decades, the 5-year overall survival of BC patients is still poorer than anticipation, especially in LncRNAs, with over 200 nucleotides in length, belong to a category of RNAs that lack the ability to encode proteins [4]. Li et al [15] discovered that lncRNA HOXC13-AS, which was significantly up-regulated in BC, enhanced cell proliferation ability through up-regulating PTEN expression via suppressing miR-497-5p
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